AB0265 Non-Canonical NF-κB Signaling in Microvessels of Atherosclerotic Lesions in Coronary Arteries Is Associated with Inflammatory Cell Infiltration and Myocardial Infarction

2016 ◽  
Vol 75 (Suppl 2) ◽  
pp. 990.2-990
Author(s):  
C.X. Maracle ◽  
R. Agca ◽  
B. Helder ◽  
H.W. Niessen ◽  
M.T. Nurmohamed ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Arteries ◽  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Atherosclerotic Lesions

scholarly journals Inhibition of the lncRNA Mirt1 Attenuates Acute Myocardial Infarction by Suppressing NF-κB Activation

2017 ◽  
Vol 42 (3) ◽  
pp. 1153-1164 ◽  
Author(s):  
Xiangrao Li ◽  
Jian Zhou ◽  
Kai Huang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Inflammatory Cell ◽  
Cultured Cells ◽  
Cardiac Fibroblasts ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Inflammatory Factors ◽  
Cardiac Functions

Background/Aims: The expression of a novel lncRNA, myocardial infarction associated transcript 1(Mirt1), has been shown to be upregulated in acute myocardial infarction (AMI). However, the role of Mirt1 in AMI is not clear. Methods: In this study, we analyzed the level of Mirt1 in cardiomyocytes and cardiac fibroblasts in AMI mice. Moreover, adenovirus mediated knockdown of Mirt1 was employed to clarify its roles in AMI mice or cultured cardiac fibroblasts. The cardiac functions and infarct size of AMI mice were examined, and tissues and cultured cells were collected and processed for histology and biochemical examination. Results: We demonstrated that Mirt1 was mainly expressed in cardiac fibroblasts, and that knockdown of Mirt1 improved cardiac functions, decreased cardiomyocytes apoptosis and attenuated inflammatory cell infiltration in vivo. Furthermore, knockdown of Mirt1 in cardiac fibroblasts not only attenuated the apoptosis of cardiomyocytes, but also suppressed the migration of macrophages under hypoxia in vitro. NF-κB signaling pathway, activated under hypoxia, was also inhibited by Mirt1 knockdown in fibroblasts. Conclusions: Knockdown of Mirt1 attenuates AMI injury presumably by decreasing cardiomyocytes apoptosis and reducing inflammatory cell infiltration. These effects could be attributed, at least partly, to inhibition of the NF-κB pathway, resulting in decreased expression of inflammatory factors.

A Case of Bullous Amyloidosis Associated with an Inflammatory Cell Infiltration and Prominent Pruritus

2008 ◽  
Vol 70 (3) ◽  
pp. 269-273
Author(s):  
Taisuke KAMIYAMA ◽  
Yoshihiro KAWAGUCHI ◽  
Masami SASAKI ◽  
Masamichi SATOU ◽  
Kumiko MIURA ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration

scholarly journals The Symmetric 3D Organization of Connective Tissue around Implant Abutment: A Key-Issue to Prevent Bone Resorption

Symmetry ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1126
Author(s):  
Giovanna Iezzi ◽  
Francesca Di Lillo ◽  
Michele Furlani ◽  
Marco Degidi ◽  
Adriano Piattelli ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Connective Tissue ◽  
Inflammatory Cell ◽  
Soft Tissues ◽  
Three Dimensional ◽  
Collagen Fibers ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Oral Epithelium ◽  
Implant Abutment

Symmetric and well-organized connective tissues around the longitudinal implant axis were hypothesized to decrease early bone resorption by reducing inflammatory cell infiltration. Previous studies that referred to the connective tissue around implant and abutments were based on two-dimensional investigations; however, only advanced three-dimensional characterizations could evidence the organization of connective tissue microarchitecture in the attempt of finding new strategies to reduce inflammatory cell infiltration. We retrieved three implants with a cone morse implant–abutment connection from patients; they were investigated by high-resolution X-ray phase-contrast microtomography, cross-linking the obtained information with histologic results. We observed transverse and longitudinal orientated collagen bundles intertwining with each other. In the longitudinal planes, it was observed that the closer the fiber bundles were to the implant, the more symmetric and regular their course was. The transverse bundles of collagen fibers were observed as semicircular, intersecting in the lamina propria of the mucosa and ending in the oral epithelium. No collagen fibers were found radial to the implant surface. This intertwining three-dimensional pattern seems to favor the stabilization of the soft tissues around the implants, preventing inflammatory cell apical migration and, consequently, preventing bone resorption and implant failure. This fact, according to the authors’ best knowledge, has never been reported in the literature and might be due to the physical forces acting on fibroblasts and on the collagen produced by the fibroblasts themselves, in areas close to the implant and to the symmetric geometry of the implant itself.

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